Abstract

ObjectiveTo determine how aggregates of intrinsic cardiac (IC) neurons transduce the cardiovascular milieu vs respond to changes in central drive. Also to determine how IC network interactions, subsequent to induced neural imbalances, subserve the genesis of atrial fibrillation (AF).MethodsActivity from multiple IC neurons within the right atrial ganglionated plexus was recorded from anesthetized canines. Induced changes in IC neuronal activity were evaluated in response to: (1) cardiac touch; (2) electrical activation of the cervical vagus or stellate ganglia; (3) occlusion of the inferior vena cava or thoracic aorta; (4) focal left ventricular ischemia and (5) neurally induced atrial arrhythmias (AF).ResultsThe majority of IC neurons were local circuit in nature and in basal states displayed low level functional interconnectivity. The majority of IC neurons received indirect central inputs (vagus and stellate) and a lesser proportion transduced the cardiac milieu including responding to multimodal stressors applied to the great vessels and heart. In response to mediastinal nerve stimulation most IC neurons became excessive excited and their functional interconnectivity enhanced; such network behavior preceding and continuing throughout AF.ConclusionStochastic interactions among IC neuronal populations underlie control of regional cardiac function. (Supported by HL71830)

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